Kidney Injury and Liver Disease - PowerPoint Presentation

Slide1

Kidney Injury and Liver Disease in the ICU

German T. Hernandez, MD, FASN, FACP

Associate Professor of Medicine

Division of Nephrology & Hypertension

Paul L. Foster School of Medicine

TTUHSC at El Paso

Slide2

Learning Objectives

1. Define the

Hepatorenal

Syndrome

2. Discuss the use of emerging medical therapies in

Hepatorenal

Syndrome

2. Recognize the abdominal compartment syndrome as cause of acute kidney injury

Slide3

Acute Kidney Injury

Many Definitions:

Increase in serum creatinine ≥1.5x baseline within 7 days (RIFLE)

or

Increase in serum creatinine by 0.3 mg/

dL or ≥1.5x baseline with 48 hrs (AKIN)

Crit

Care 2004; 8:B204

Crit

Care 2001; 11:R31

Slide4

Acute Kidney Injury: Classification

Prerenal

AKI

Intrinsic AKI

Acute Tubular Necrosis (ATN)

Interstitial NephritisGlomerulonephritisVascular syndromesIntra-tubular obstruction

(crystals,

myeloma casts)

Post-renal AKI

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Acute Kidney Injury in Liver Disease

Caveat:

Renal dysfunction in liver disease may go unrecognized

Decreased creatinine and urea production

A normal serum creatinine (1.0-1.3) may represent a low glomerular filtration rate (

eGFR

)

Am J Med 1987; 82:945

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Prerenal AKIATN

Hepatorenal

Syndrome

Interstitial Nephritis

Glomerular Diseases

MPGN (Hep C)IgA nephritisMembranous nephropathy (

Hep

B)

Cryoglobulinemia

(

Hep

C)

Acute Kidney Injury in Liver Disease

Slide7

Hepatorenal Syndrome

F

unctional renal failure caused by

intrarenal

vasoconstriction in patients with ESLD

Splanchnic vasodilatationRelatively low cardiac output

Effective circulatory

hypovolemia

Gut 2007; 56:1310-1318

Slide8

HRS typically presents with:Oliguria

Benign urine sediment

Very low urine Na excretion

Progressive rise in serum creatinine

(may have periods of stabilization)

Hepatorenal

Syndrome

Gut 2007; 56:1310-1318

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Pathophysiology

Slide10

HRS Diagnostic Criteria

HRS is a diagnosis of exclusion

Cirrhosis with ascites

Serum Creatinine > 1.5 mg/

dL

No improvement in SCr (<1.5 mg/dL

) after at least 2 days of diuretic withdrawal and IV albumin (1g/kg/day, max 100g/day)

Absence of shock

No intrinsic renal disease: proteinuria >500mg/day, >50 RBC/HPF, or abnormal renal US

Gut 2007; 56:1310-1318

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Hepatorenal Syndrome

Type-1 HRS

Rapid progression of kidney injury with a rise in

SCr

>2x baseline in less than 2 weeks

Can develop spontaneously, but commonly follows:SBP or other infection

GI bleeding

Gut 2007; 56:1310-1318

Slide12

Hepatorenal Syndrome

Type-2 HRS

Associated with diuretic-resistant ascites and less renal insufficiency than type-1 HRS

Gut 2007; 56:1310-1318

Slide13

Outcomes in HRS

Gut 2007; 56:1310-1318

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HRS: Treatment

Liver transplantation for both type 1 and 2 HRS

Vasoconstrictors for type 1 HRS

Terlipressin

Norepinephrine

Midodrine/octreotide

TIPS

Slide15

HRS Type 1: Terlipressin & Albumin

Terlipressin

: vasopressin analog, reduces splanchnic vasodilatation

Dosing: 1-2 mg IV every 4hrs

Given with IV Albumin 1g/kg, then 20-40g/day

Significant improvement in renal function

Not available in the USA

No difference in survival at 3 months vs. albumin alone

Survival benefit for renal responders

Gastroenterology 2008; 134:1352-9

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Renal Response: Terlipression+Albumin

vs

Albumin alone

Gastroenterology 2008; 134:1352-9

Slide17

HRS-1: Norepinephrine

Uncontrolled pilot study, n=12

Norepinephrine 0.5-3mg/

hr

with IV albumin and furosemide

Hepatology

2002; 36:374-380

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HRS-1: Midodrine & Octreotide

Midodrine

- selective alpha-1 adrenergic agonist

Causes increase in peripheral vascular resistance

Octreotide

-analogue of

somatostatin

Inhibits endogenous vasodilator release, thereby reducing splanchnic vasodilatation

The combination is thought to improve renal and systemic hemodynamics

Slide19

HRS-1: Midodrine & Octreotide

Group A: 8 subjects treated with

Dopamine 2-4mcg/kg/min

Group B: 5 subjects treated with

Midodrine

7.5-12.g mg

po

TID

Octreotide

100-200 mcg

subq

TID

Both meds titrated to an increase in MAP of ≥ 15 mmHg

Both groups also received IV Albumin

Hepatology

1999; 29:1690-7

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Dopamine vs. Midodrine+Octreotide

Hepatology

1999; 29:1690-7

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Dopamine vs. Midodrine+Octreotide:

Survival

Hepatology

1999; 29:1690-7

Slide22

Abdominal Compartment Syndrome

Intra-abdominal hypertension

Intra-abdominal pressure ≥ 12 mmHg; (normal 5-7 mmHg) or

Abdominal perfusion pressure <60 mmHg

APP=MAP-IAP

Abdominal compartment syndromeIAP ≥ 20 mmHg and new organ dysfunction

Intensive Care Med 2006; 32:1722

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Slide24

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Abdominal Compartment Syndrome

Systemic effects

Impaired cardiac function (from compression due to elevation of diaphragm); reduced venous return

Increased intra-thoracic pressures, risk of barotrauma, etc.

Decreased splanchnic perfusion

Decreased hepatic ability to metabolize lactic acid

Increase in ICP

Intensive Care Med 2006; 32:1722

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Abdominal Compartment Syndrome

Renal effects

Acute kidney injury due to:

Renal vein compression with higher venous resistance and impaired venous drainage

Renal artery vasoconstriction via overactive sympathetic drive and renin-angiotensin axis

Drop in GFR

Drop in urine output: Oliguria with IAP 15 mmHg, anuria with IAP 30 mmHg

Decreased urine sodium and chloride

Trauma 2000; 48:874

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Abdominal Compartment Syndrome

Clinical settings in which to keep ACS in mind

Trauma patients following aggressive volume resuscitation

Burn patients >30% BSA

Post liver transplant

Massive ascites, bowel distention, abdominal

surgery,

intraperitoneal

bleeding

Ruptured AAA, pelvic

fx

with bleeding, pancreatitis

Crit

Care Med 2005; 33:315

Crit

Care Med 2004; 30:822

Slide28

Abdominal Compartment Syndrome

Diagnosis

First of all think of the diagnosis

Measure IAP

Treatment

Abdominal Decompression

Renal dysfunction is generally reversible if decompression is done in a timely manner

Trauma 2000; 48:874

Arch Intern Med 1985; 145:553

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The End

Thank you for

your attention